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Carbidopa inhibits aromatic-L-amino-acid decarboxylase (DOPA Decarboxylase or DDC), an enzyme important in the biosynthesis of L-tryptophan to serotonin and in the biosynthesis of L-DOPA to Dopamine (DA). Along with carbidopa, other DDC inhibitors are benserazide (Ro-4-4602), difluromethyldopa, and α-methyldopa.
Used in tandem with L-DOPA (trade name levodopa, a dopamine precursor converted in the body to dopamine), it increases the plasma half-life of levodopa from 50 minutes to 1 1/2 hours. CarbiDOPA cannot cross the blood brain barrier, so it inhibits only peripheral DDC. It thus prevents the conversion of L-DOPA to dopamine peripherally. This reduces the side effects caused by dopamine on the periphery, as well as increasing the concentration of L-DOPA and dopamine in the brain.
Carbidopa is also used in combination with 5-HTP, a naturally-occurring amino acid which is a precursor to the neurotransmitter serotonin and an intermediate in tryptophan metabolism. Carbidopa prevents 5-HTP's metabolism in the liver, which can lead to elevated levels of serotonin in the bloodstream. Research shows that co-administration of 5-HTP and carbidopa greatly increases plasma 5-HTP levels.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Carbidopa". A list of authors is available in Wikipedia.|